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Since the early years of its discovery, Ameri-can trypanosomiase has been seen as a disease dueto indirect damage via inflammation due to theimmune response of a host against systemic tissuecolonization by the Trypanosoma cruzi (Vianna1911, Magarinos Torres 1928). The expression ofthis immune response has been studied over thecentury, but the mechanisms involving the patho-genesis of this disease are not well understood andremain a matter of debate (Kierszenbaum 1985,Hudson 1985).Although there are many difficulties in corre-lating the chronic form of the disease in mice andhumans, the mouse model has been the most stud-ied. In addition, experimental American trypano-somiasis in mice has been proposed as a model forthe study of autoimmune diseases. It has been em-phasized that T. cruzi infections in mice offer anattractive means of investigation for the inductionof autoimmunity and its consequences by (1) shar-ing of antigenic determinants (Acosta et al. 1985);(2) alteration of host cells surfaces by adsorptionof T. cruzi released antigens (Muniz et al. 1970,Ribeiro dos Santos & Hudson 1980 a,b); (3) ex-pressing parasite antigens on the surface of infectedcells (Araujo 1985).Moreover the parasite can invade either theprimary (Savino et al. 1989, Goncalves da Costaet al. 1991) or the secondary lymphoid organs(Brener & Chiari 1963, Goncalves da Costa et al.1984) transforming them into target organs sinceparasite antigens may transform the microenviron-ment and induce the destruction of transformedcells by cytotoxic lymphocytes. This process wasdescribed acting against sensitized neurons andmuscle fibers (Kuhn & Mumane 1977), but it mayoccur systemically. Systemic infection occurs inimmunocompromised hosts (Goncalves da Costaet al. 1984) as well as in normal ones (Lenzi et al.1996). The systemic and intense infection observedin mice has a correlation with severe clinical casesdescribed in man by Chagas (1916), who wasworking mostly with children.The balance of host/parasite relationship ap-pears in some instances as the intensity of inflam-matory infiltrate versus the parasite load. Experi-mental models allow the development of two po-lar expressions of this relationship: (1) absence ofan inflammatory reaction in athymic nude mice;(2) an enhancement of myocarditis in infected micewhere cyclophosphamide is given two days beforeinfection (Goncalves da Costa et al. 1984,Calabrese et al. 1996). An enhancement of myo-carditis has been also observed in dogs after CYtreatment (Andrade et al. 1987).Immunomodulation can alter the flux of inflam-matory cells to the site where the parasite or itsantigens persist as well as the nature of the inflam-matory type and subsets.Contradictory results have been reported in dif-ferent experimental studies upon superinfections.More severe lesions have been reported histo-pathologicaly in superinfections than in prime-in-fected mice (Fernandes et al. 1966), while otherauthors have shown very similar lesions in bothgroups in assays using genetically characterized T.cruzi clones (Lauria-Pires & Teixeira 1996).Recently, it has been observed that mice thatbecome chronically infected by a vaccination pro-cedure using BCG associated with T. cruzi flagel-lar fraction antigens present a severe myosite aftera superinfection with the same strain. This inflam-matory infiltrate has shown a significant partici-pation of eosinophils in comparison with lesionsof prime-infected mice (manuscript in preparation).Little information has been brought out by the au-thors, but the occurrence of eosinophilia in the laststages of the acute period of infection was reportedin patients by Emanuel Dias (1912). The role ofeosinophils in antibody-dependent cellularcytotoxity (ADCC) has been reported in in vitro

Mouse as a model for Chagas disease: does mouse represent a good model for Chagas disease?